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Biomedical subjects

W A Pryor

Publications and source records attributed to W A Pryor.

At least 127 records · Page 7Linked to original sources
PubMed1989

Quantitative analysis of the hydrogen peroxide formed in aqueous cigarette tar extracts.

We have established, for the first time, a reliable method to quantitate hydrogen peroxide (H2O2) generated in aqueous extracts of cigarette smoke tar. The aqueous tar extract was passed through a short reverse-phase column and its H2O2 concentration determined by differential pulse polarography using an automatic reference subtraction system. The H2O2 concentration increased with aging, pH and temperature; the presence of superoxide dismutase lead to lower H2O2 concentrations. This method was applied to many kinds of research and commercial cigarettes. With a few exceptions, the amount of H2O2 formed after a fixed time from each cigarette smoke was proportional to its tar yield.

Hydrogen Peroxide↗
PubMed1989

Persistent free radicals in woodsmoke: an ESR spin trapping study.

Free radicals are detected in the gas-phase smoke resulting from the combustion of wood using the electron spin resonance (ESR) spin trapping method. The materials were pyrolyzed by rapid heating in a quartz tube in a flowing air stream. The filtered smoke was bubbled into a dodecane solution of alpha-phenyl-N-tert-butyl nitrone, and the resulting nitroxide radicals were detected by ESR. The radicals spin trapped from woodsmoke are compared to those we have spin trapped from tobacco smoke; the smoke from both yellow pine and oak produce more intense ESR spectra than does tobacco smoke per unit mass burned under the conditions of these experiments. When woodsmoke is bubbled through pure dodecane and the resulting woodsmoke/dodecane solution is held for a delay time before the PBN is added, radicals are detected even after the woodsmoke/dodecane solution is aged for more than 20 min. Similar experiments with tobacco smoke show that radicals no longer are trapped even after much shorter delay times from tobacco smoke/dodecane solutions.

Electron Spin Resonance Spectroscopy↗
PubMed1988

Why is the hydroxyl radical the only radical that commonly adds to DNA? Hypothesis: it has a rare combination of high electrophilicity, high thermochemical reactivity, and a mode of production that can occur near DNA.

Free radicals do not commonly add to nucleotides in DNA, despite the fact that radicals are produced in all aerobically metabolizing cells. Why is this? For oxy-radicals, the ratio of the rate constant for addition to double bonds divided by that for H-abstraction from good H-donors parallels the electrophilicity of the radical, and among oxy-radicals the hydroxyl radical is the most electrophilic, with an unusually high ratio of Kad/kH. The hydroxyl radical also is very reactive in H-atom abstraction reactions, with a large absolute value of kH. However, the hydroxyl radical's high reactivity makes it unselective and relatively nondiscriminating between H-abstraction from a sugar moiety in DNA and penetration to, and reaction with, a base. Oxy-radicals such as alkoxyl and peroxyl radicals do not have as high electrophilicity or as high reactivity. Interestingly, carbon-centered radicals (such as the methyl radical) also can both add to double bonds and abstract H-atoms, but carbon-centered radicals are not commonly observed to add to DNA bases. However, they cannot be generated near DNA in vivo. In contrast, hydroxyl radical generating systems appear to complex with DNA and produce the hydroxyl radical in the immediate vicinity of the DNA, producing a type of DNA damage that is called site specific. Thus, addition of a radical to a DNA base may require all three features possessed by the hydroxyl radical: high electrophilicity, high thermokinetic reactivity, and a mechanism for production near DNA.

DNA↗
PubMed1988

Persistent free radicals in the smoke of common household materials: biological and clinical implications.

We have detected free radicals in the gas-phase smoke resulting from the combustion of several household materials. Materials were pyrolyzed by rapid heating in a quartz ignition tube in a flowing air stream. The filtered smoke was bubbled into a dodecane solution of alpha-phenyl-N-t-butylnitrone (PBN), and the resulting nitroxide radicals were detected by electron spin resonance. Cellulosic materials (birch plywood, cellulose, 1R1 research cigarette tobacco, and yellow pine) and dried exterior paint produce about the same yield of trapped radicals. The smoke from polyethylene and rubber produce approximately 2-fold more radicals than the smoke from the cellulosic materials. Nylon smoke yields about 10-fold less radicals than the cellulosic materials. The smokes from polyvinyl chloride and polytetraflouroethylene do not produce detectable spin adducts of PBN by this method. Where radicals were trapped, oxygen-centered spin adducts predominated; lesser amounts of carbon-centered spin adducts and an oxidation product of PBN were observed. Different oxygen-centered radicals were detected from different materials, as judged from the variation observed in the hyperfine splitting constants of the principal spin adducts. When cellulose smoke is dissolved in solution, radicals continue to be produced for at least 20 min, suggesting the production of a metastable species in the gas phase that decomposes to form radicals in solution.

Cellulose↗
PubMed1988

Toxicity of polycyclic aromatic hydrocarbons. VI. Effects of 1-nitropyrene on serum enzyme levels in rats, and protection against it by beta-naphthoflavone and dimethyl sulfoxide.

Male Sprague-Dawley rats were pretreated i.p. with corn oil or DMSO (1.5 ml/kg/day), or with beta-naphthoflavone (BNF, 40 mg/kg/day) in corn oil or DMSO for 3 days. 1-Nitropyrene (1-NP, 150 mg/kg) in DMSO was injected i.p. 24 hr after pretreatment. A significant increase in the levels of several serum enzymes was seen in rats pretreated with corn oil alone 24 hr after 1-NP injection. The increase in enzyme activities was significantly reduced by a 3-day pretreatment with DMSO or BNF.

Alanine Transaminase↗
PubMed1988

Toxicity of aromatic hydrocarbons. VII. Hepatotoxicity of 9-nitrophenanthrene, and protection against it by beta-naphthoflavone.

Male Sprague-Dawley rats were treated with a single i.p. injection of DMSO (3.0 ml/kg) or 9-nitrophenanthrene (9-NP, mg/kg) in DMSO. 9-NP produced a significant elevation of serum aspartate aminotransferase, alanine aminotransferase, sorbitol dehydrogenase, and gamma-glutamyl transpeptidase (GGTP) levels relative to DMSO-injected rats 24 hr after injection. With the exception of GGTP, the increase in enzyme activities induced by 9-NP was significantly reduced by a 3-day pretreatment with beta-naphthoflavone (BNF; 40 mg/kg/day) in DMSO. The effect of 9-NP on GGTP levels was enhanced by BNF pretreatment.

Alanine Transaminase↗
PubMed1987

The kinetics of the autoxidation of polyunsaturated fatty acids.

The kinetics of the autoxidation of a series of polyunsaturated fatty acids (PUFA) with increasing degrees of unsaturation and the mono-, di- and triglycerides of linoleate have been studied in homogeneous chlorobenzene solution at 37 C under 760 torr of oxygen. The autoxidations were initiated by thermal decomposition of azo initiators and followed by measuring the rate of oxygen uptake. The rate of chain initiation was determined by the induction period method using alpha-tocopherol as the chain-breaking antioxidant. The measured oxidizabilities of the PUFA are linearly dependent on the number of doubly allylic positions present in the molecule. Thus, the oxidizability of linoleate is 2.03 X 10(-2) M-1/2 sec-1/2, and the value for docosahexaenoate is five times greater, 10.15 X 10(-2) M-1/2 sec-1/2. The rate of autoxidation for all PUFA studied and for the mono- and diglyceride is proportional to the substrate concentration and to the square root of the rate of chain initiation, implying that the autoxidation of these compounds follows the usual kinetic rate law. The autoxidation of the triglyceride is more complex and does not appear to follow the same rate law at all substrate concentrations. This deviation from the usual kinetic rate expression may be due to lipid aggregation at low concentrations of the triglyceride.

Chemical Phenomena↗
PubMed1987

Views on the wisdom of using antioxidant vitamin supplements.

In the Forum that follows, four authorities in nutrition and vitaminology present their divergent views on the use of antioxidant vitamin supplements. In this introduction, the basic dilemma between setting RDAs that insure an absence of deficiency symptoms and those that insure optimal health is discussed, as well as other factors that must be considered to reach a consensus on this controversial topic.

Antioxidants↗
PubMed1987

DNA synthesis is blocked by cigarette tar-induced DNA single-strand breaks.

DNA single-strand breaks are caused by aqueous extracts of cigarette tar, due to the reduction of oxygen to superoxide by tar and the subsequent production of hydroxyl radicals. The action of DNA metabolism enzymes on these single-strand breaks has been studied to probe the consequences of these lesions for DNA repair. Our results demonstrate that cigarette tar-induced nicks are blocked at the 3' terminus since they are totally incapable of activating DNA for DNA synthesis by Escherichia coli DNA polymerase I. The 3' termini of these tar-induced nicks are activated, however, for DNA synthesis by E. coli exonuclease III or by the 3' phosphatase activity of T4 polynucleotide kinase. Because of the inability of tar-induced lesions to support DNA synthesis, they probably require a multi-step process for repair in vivo. As a consequence, the overall likelihood of mutation is increased due to the possibility for error at each step of the repair process.

Bacteriophages↗
PubMed1987

Oxygen radicals and human disease.

Toxic oxygen free radicals have been implicated as important pathologic mediators in many clinical disorders. We discuss the chemistry of oxygen radical production and the roles of iron and of various antioxidants as well as the diseases that have received active attention in oxy-radical research. Particular attention is focused on cigarette smoke oxidants, ischemia-reperfusion-induced radical production, carcinogenesis, and aging. Such research may well provide a firm foundation for therapeutic breakthroughs.

Aging↗
PubMed1987

Toxicity of polycyclic aromatic hydrocarbons. IV. Effects of diphenaldehyde, a major product of ozonized phenanthrene, in rats.

Diphenaldehyde is the major product of phenanthrene ozonized on silica gel. Male Sprague-Dawley rats were treated with a single ip injection of DMSO (3.0 ml/kg) or diphenaldehyde (90 mg/kg) in DMSO. Diphenaldehyde produced significant alterations in levels of serum aspartate aminotransferase, alanine aminotransferase, sorbitol dehydrogenase, gamma-glutamyl transpeptidase, and lactate dehydrogenase relative to DMSO-injected rats 24 hr after injection. These results, as well as gross observations on necropsy, suggest that diphenaldehyde exhibits significant hepatotoxicity.

Alanine Transaminase↗
PubMed1987

Toxicity of polycyclic aromatic hydrocarbons. V. Protective effect of beta-naphthoflavone against hepatotoxicity induced by diphenaldehyde in rats.

Male Sprague-Dawley rats were treated ip with beta-naphthoflavone (40 mg/kg/day) in corn oil or in DMSO for three days. Diphenaldehyde (90 mg/kg in DMSO) was injected ip 24 hr after pretreatment. The increase in the levels of aspartate aminotransferase, alanine aminotransferase, sorbitol dehydrogenase, gamma glutamyl transpeptidase, and lactate dehydrogenase was significantly lower in rats pretreated with BNF. This suggests that the BNF-induced P-450 isozyme systems have a protective effect against the acute hepatotoxicity of diphenaldehyde.

Aldehydes↗
PubMed1987

Toxicity of polycyclic aromatic hydrocarbons. III. Effects of beta-naphthoflavone pretreatment on hepatotoxicity of compounds produced in the ozonation or NO2-nitration of phenanthrene and pyrene in rats.

Male Sprague-Dawley rats were treated ip with beta-naphthoflavone (BNF, 40 mg/kg/day) in dimethylsulfoxide (DMSO, 26.7 mg BNF/ml) for three days. At 24 hr after the pretreatment DMSO (3.0 ml/kg), phenanthrene (150 mg/kg), ozonized or nitrated products of phenanthrene (150 mg/kg), pyrene (150 mg/kg), or ozonized or nitrated products of pyrene (150 mg/kg) were injected ip. Phenanthrene, pyrene, and their ozonized or nitrated products were dissolved in DMSO (50 mg/ml). No increase in the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT) or sorbitol dehydrogenase (SDH) was seen in the pretreated rats 48 hr after the treatment. This is in contrast to what was seen in previous work without the BNF pretreatment. BNF pretreatment induced a small but significant increase in gamma-glutamyl transpeptidase (GGTP) levels. No treatment group receiving BNF differed from another with respect to GGTP. A decrease in lactate dehydrogenase (LDH) levels was noted in the nitro-PAH treatment groups; the same phenomenon was observed earlier in rats treated with nitro-PAH without BNF treatment. These results suggest that the mixed-function oxidase systems specifically induced by BNF have a protective effect against the hepatotoxicity of the oxonized or nitrated products of phenanthrene and pyrene.

Animals↗
PubMed1987

Toxicity of polycyclic aromatic hydrocarbons. II. Effect of NO2-nitrated phenanthrene and pyrene on blood chemistry in rats.

Male Sprague-Dawley rats were treated with a single ip injection of dimethyl sulfoxide (DMSO), phenanthrene, nitrated products of phenanthrene, pyrene, or nitrated products of pyrene. Phenanthrene, pyrene and their nitrated products were dissolved in DMSO. Phenanthrene produced a significant elevation of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels relative to DMSO-injected rats 24 hr after injection. Gamma-glutamyl transpeptidase (GGTP) levels were significantly increased for groups treated with phenanthrene when compared with the DMSO group 72 hr after injection. Nitrated products of phenanthrene produced a significant elevation of serum AST, ALT, sorbitol dehydrogenase (SDH), and GGTP levels when compared with groups treated with DMSO and phenanthrene 24 hr after injection. Four of six rats in the nitrated phenanthrene treatment group died between 48 and 72 hr after the injection. Injection of pyrene caused no significant increases in serum enzyme activities. Significant changes in the serum AST, SDH and LDH levels were observed with the nitrated products of pyrene at 24 hr. Only SDH levels were significantly different when pyrene and its nitrated products were compared. No significant differences were detected at 72 hr with the nitrated products of pyrene. As supported by serum chemistry, this study suggests that the products of the reaction of NO2 with two model polynuclear aromatic hydrocarbons (PAH) are hepatotoxic. Both pyrene and phenanthrene form nitrated products that are more toxic than the parent PAH, but the nitrated products of phenanthrene appear to be more toxic than the nitration products of pyrene.

Animals↗